SUMMARY1. Pulsed bidirectional Doppler-ultrasound equipment was used to measure changes in blood velocities in the femoral artery on a beat to beat basis for consecutive contraction and relaxation phases during voluntary rhythmic exercise of the quadriceps muscle group in man.2. Rapid and large fluctuations of blood velocities were found, being high during relaxation and low during contraction phases. At the onset of contraction phase, negative velocities were present, indicating retrograde flow. During the rest of the contraction phase, forward flow occurred comparable to the resting flow level even at high loads.3. Estimated maximal flow to the whole leg during relaxation phase, calculated from these blood velocity measurements and vessel diameter (measured with echoultrasound equipment with high resolution) was in two of the subjects 3-32 1 min-' (female) and 5.97 1 min-1 (male). When using computer tomography to estimate the volume of the quadriceps muscle group, the calculated maximum flow to this muscle group was 243 (female) and 257 (male) ml min-' 100 ml muscle-'. The time-averaged flow during exercise to the whole leg was 1-51 1 min-' (female) and 2'47 1 min-(male). The calculated time-averaged flow to the quadriceps muscle group was 101 (female) and 98 (male) ml min-' 100 ml muscle-'.4. The duration of post-contraction hyperaemia following such rhythmic exercise of up to 6 min duration and up to 75 % maximum voluntary contraction was never in excess of 150 s.
SUMMARY1. Blood velocities in the human femoral artery were measured using pulsed bidirectional Doppler-ultrasound equipment before, during and after single isometric contractions of the quadriceps muscle group.2. After contraction periods lasting more than 20 s (long) and of tensions from 10 % up to 75 % of maximal voluntary contraction (m.v.c.), an increase in blood velocities of seven to eight times the resting level was observed. Estimated maximal volume flow to the whole leg during the post-contraction hyperaemic phase calculated from these blood velocity measurements and vessel diameter (measured with echoultrasound equipment) was in two of the subjects 2-4 1/min (female) and 4-4 1/min (male), respectively. In the latter, this estimate fitted very well with results obtained using a venous thermo-dilution method. When using computer tomography to estimate the volume of the quadriceps muscle group, the calculated maximum flow to this muscle group in the post-contraction hyperaemic phase was approximately 175 (female) and 185 (male) ml/min. 100 ml muscle, respectively. This was about forty times the estimated resting volume flow to this muscle of 4-7 (female) and 4'5 (male) ml/min. 100 ml muscle.3. The length of the post-contraction hyperaemia after short (< 10 s) contraction periods was 12-13 s, by which time velocities had reached 25 % above the precontraction level. After long contractions, the corresponding values were 23-25 s. By contrast, previous plethysmographic observations by others indicate that postcontraction hyperaemias following long contractions last 10-15 min.4. There was a marked difference between the times taken to reach maximal velocity in the hyperaemic phase when comparing short and long contractions. Maximal velocity was reached four to six cardiac cycles following short periods of contraction but during the very first heart beat after long periods of contractions. 5. The present observations are compatible with the hypothesis that locally released metabolites or hormones play a dominant role in the regulation of the post-contraction hyperaemia. Since during the short contraction periods maximal velocity was reached only after some seconds, whereas with the longer contraction periods it was reached during the first heart beat, it is suggested that these metabolites are released at some distance from the resistance vessels and that some time is needed for diffusion.
SUMMARY1. An improved Doppler ultrasound technique was used to measure stroke volume (SV) and cardiac output (CO) on a beat-to-beat basis in a group of supine humans before, during and after periods of standardized, rhythmic exercise, involving the quadriceps muscle groups on both sides. The development of CO on such bouts of exercise was compared to Doppler ultrasound records of the simultaneous femoral arterial flow (FF) response.2. Records of CO at rest revealed spontaneous fluctuations around a mean level, with differences between the minimal and maximal values of the order of 11 min'. The mean CO level at rest again varied considerably from one day to another and from test run to test run.3. Upon start of exercise an immediate and rapid increase in heart rate (HR) and CO took place. The entire increase, the size of which varied appreciably from test run to test run, was completed within 10-15 s. No or only minor changes were seen in the mean SV level during the exercise periods.4. The time course of the increase in FF was indistinguishable from that of the increase in CO, which occurred without any detectable delay relative to the changes in FF. These closely parallel developments indicate a tight regulatory coupling between the two types of flow changes.5. In the majority of tests the total and two-sided increase in FF seen in the steady-state situation in the last part of an exercise period was significantly larger than the recorded increase in CO. This discrepancy implies that some redistribution of flow from tissues other than the working muscles might take place, even at this moderate level of work.
We examine whether muscle oxygen consumption (VO2) increases gradually during repeated submaximal isometric contractions. Six subjects made two-legged isometric quadriceps contractions at 30% maximal voluntary contraction for 6 s with 4 s of rest between until exhaustion (58 +/- 8 min). Blood samples were taken from the femoral vein and artery, and blood velocity was recorded by ultrasound-Doppler technique in the femoral artery. Blood flow was calculated from velocity and artery diameter values. Leg VO2 increased sixfold within the 1st min of exercise. A further doubling of the VO2 was seen during the remainder of the exercise, reaching 307 +/- 22 ml/min at exhaustion. This latter increase was due to a 54% increase in blood flow and a 34% increase in oxygen extraction. After 20 min of recovery VO2 was still 75% higher than preexercise values. The results show a twofold increase in energy demand of the working muscle during repeated constant-force isometric contractions. The increased energy cost of contraction is probably localized at the cellular level, and it parallels fatigue determined as decreased force-generating capacity.
BackgroundThe VascuQoL-6 (VQ-6) health-related quality of life questionnaire, a short version of the disease-specific VascuQoL-25, was developed for clinical practice and use in vascular registries. The study purpose was to evaluate the validity and reliability of VQ-6.MethodsVQ-6 was translated to Norwegian with linguistic validation and face value evaluation, and consecutive patients with intermittent claudication (IC) or critical limb ischemia (CLI) were included. All patients completed VQ-6 and Short Form-36 (SF-36), and were evaluated with ankle-brachial index (ABI) measurement pre- and post-exercise, a constant load treadmill test and clinical consultation at baseline and after 4 weeks. Correlation analysis, change statistics and receiver operator characteristics (ROC) curves were used to evaluate reliability, validity and responsiveness to change.ResultsOne hundred seventy-one patients with peripheral arterial disease (PAD) were included, 70 (41%) female. 147 (86%) of the patients suffered from IC. The reliability of VQ-6 was good, Cronbachs-α 0.82. The ability of VQ-6 to differentiate between IC and CLI was good, area under the curve (AUC) 0.754. There was good correlation between SF-36 physical domains and component scores and VQ-6 score (r = 0.55–0.62) and excellent responsiveness to change after treatment, standard response mean (SRM) 1.12. The clinical anchors of ABI at rest, treadmill walking performance and Fontaine class improvement were less responsive to change than VQ-6, SF-36 and the vascular surgeon’s evaluation.ConclusionsVQ-6 is reliable and valid, and can be used to evaluate PAD treatment in clinical practice and in vascular registries. Further research is necessary to determine the clinically important change over time.Trial registration ISRCTN14846962 (retrospectively registered).
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